• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Vascular smooth muscle cell-derived, Gla-containing growth-potentiating factor for Ca(2+)-mobilizing growth factors.

作者信息

Nakano T, Higashino K, Kikuchi N, Kishino J, Nomura K, Fujita H, Ohara O, Arita H

机构信息

Shionogi Research Laboratories, Shionogi & Co., Ltd., Osaka, Japan.

出版信息

J Biol Chem. 1995 Mar 17;270(11):5702-5. doi: 10.1074/jbc.270.11.5702.

DOI:10.1074/jbc.270.11.5702
PMID:7890695
Abstract

Proliferation of vascular smooth muscle cells (VSMC) is triggered by two types of growth factors. One activates tyrosine kinase-type receptors and the other activates G-protein-coupled receptors. We found that a conditioned medium of rat VSMC contained a growth-potentiating activity for the latter type of growth factor, and we purified a 70-kDa growth-potentiating factor (GPF) from the conditioned medium. Analyses of GPF and its cDNA revealed GPF to be a gamma-carboxyglutamic acid-containing protein encoded by a growth arrest-specific gene, gas6, which related to protein S. GPF specifically potentiated cell proliferation mediated by Ca(2+)-mobilizing receptors. The presence of a specific binding site suggests that the effect of GPF is mediated by a receptor. Thus, GPF may be a new type of extracellular factor regulating VSMC proliferation.

摘要

相似文献

1
Vascular smooth muscle cell-derived, Gla-containing growth-potentiating factor for Ca(2+)-mobilizing growth factors.
J Biol Chem. 1995 Mar 17;270(11):5702-5. doi: 10.1074/jbc.270.11.5702.
2
Requirement of gamma-carboxyglutamic acid residues for the biological activity of Gas6: contribution of endogenous Gas6 to the proliferation of vascular smooth muscle cells.γ-羧基谷氨酸残基对Gas6生物活性的需求:内源性Gas6对血管平滑肌细胞增殖的作用
Biochem J. 1997 Apr 15;323 ( Pt 2)(Pt 2):387-92. doi: 10.1042/bj3230387.
3
Epiregulin is a potent vascular smooth muscle cell-derived mitogen induced by angiotensin II, endothelin-1, and thrombin.表皮调节素是一种由血管紧张素II、内皮素-1和凝血酶诱导产生的强效血管平滑肌细胞源性促有丝分裂原。
Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1633-8. doi: 10.1073/pnas.96.4.1633.
4
Characterization of a high-affinity and specific binding site for Gas6.
FEBS Lett. 1996 May 27;387(1):75-7. doi: 10.1016/0014-5793(96)00394-8.
5
G-protein coupled and tyrosine kinase receptors: evidence that activation of the insulin-like growth factor I receptor is required for thrombin-induced mitogenesis of rat aortic smooth muscle cells.G蛋白偶联受体和酪氨酸激酶受体:凝血酶诱导大鼠主动脉平滑肌细胞有丝分裂需要胰岛素样生长因子I受体激活的证据。
J Clin Invest. 1996 Jan 1;97(1):139-45. doi: 10.1172/JCI118381.
6
cGMP-elevating agents suppress proliferation of vascular smooth muscle cells by inhibiting the activation of epidermal growth factor signaling pathway.环磷酸鸟苷(cGMP)升高剂通过抑制表皮生长因子信号通路的激活来抑制血管平滑肌细胞的增殖。
Circulation. 1997 Mar 4;95(5):1269-77. doi: 10.1161/01.cir.95.5.1269.
7
G protein-coupled receptors control vascular smooth muscle cell proliferation via pp60c-src and p21ras.G蛋白偶联受体通过pp60c-src和p21ras控制血管平滑肌细胞增殖。
Am J Physiol. 1997 Jun;272(6 Pt 1):C2019-30. doi: 10.1152/ajpcell.1997.272.6.C2019.
8
COP-1, a member of the CCN family, is a heparin-induced growth arrest specific gene in vascular smooth muscle cells.结缔组织生长因子-1(COP-1)是CCN家族的成员之一,是血管平滑肌细胞中肝素诱导生长停滞特异性基因。
J Cell Physiol. 2001 Jul;188(1):45-55. doi: 10.1002/jcp.1100.
9
Heparin rapidly and selectively regulates protein tyrosine phosphorylation in vascular smooth muscle cells.
J Cell Physiol. 1999 Feb;178(2):205-15. doi: 10.1002/(SICI)1097-4652(199902)178:2<205::AID-JCP10>3.0.CO;2-9.
10
Inhibition of tyrosine phosphorylation prevents thrombin-induced mitogenesis, but not intracellular free calcium release, in vascular smooth muscle cells.
J Biol Chem. 1992 Mar 15;267(8):5608-13.

引用本文的文献

1
Gas6 induces AIM to suppress acute lung injury in mice by inhibiting NLRP3 inflammasome activation and inducing autophagy.Gas6通过抑制NLRP3炎性小体激活和诱导自噬,诱导AIM抑制小鼠急性肺损伤。
Front Immunol. 2025 Feb 17;16:1523166. doi: 10.3389/fimmu.2025.1523166. eCollection 2025.
2
Modification of Gas6 Protein in the Brain by a Functional Endogenous Tissue Vitamin K Cycle.脑内 Gas6 蛋白的功能内源性组织维生素 K 循环修饰。
Cells. 2024 May 18;13(10):873. doi: 10.3390/cells13100873.
3
Circulating small extracellular vesicles promote proliferation and migration of vascular smooth muscle cells via AXL and MerTK activation.
循环的小细胞外囊泡通过 AXL 和 MerTK 的激活促进血管平滑肌细胞的增殖和迁移。
Acta Pharmacol Sin. 2023 May;44(5):984-998. doi: 10.1038/s41401-022-01029-8. Epub 2022 Nov 30.
4
Gas6 Ameliorates Inflammatory Response and Apoptosis in Bleomycin-Induced Acute Lung Injury.Gas6改善博莱霉素诱导的急性肺损伤中的炎症反应和细胞凋亡。
Biomedicines. 2021 Nov 12;9(11):1674. doi: 10.3390/biomedicines9111674.
5
Phosphatidylethanolamine and Phosphatidylserine Synergize To Enhance GAS6/AXL-Mediated Virus Infection and Efferocytosis.磷脂酰乙醇胺和磷脂酰丝氨酸协同作用增强 GAS6/AXL 介导的病毒感染和胞吐作用。
J Virol. 2020 Dec 22;95(2). doi: 10.1128/JVI.02079-20.
6
Regulation of Energy Metabolism by Receptor Tyrosine Kinase Ligands.受体酪氨酸激酶配体对能量代谢的调节
Front Physiol. 2020 Apr 21;11:354. doi: 10.3389/fphys.2020.00354. eCollection 2020.
7
AXL Receptor Tyrosine Kinase as a Therapeutic Target in Hematological Malignancies: Focus on Multiple Myeloma.AXL受体酪氨酸激酶作为血液系统恶性肿瘤的治疗靶点:聚焦于多发性骨髓瘤
Cancers (Basel). 2019 Nov 5;11(11):1727. doi: 10.3390/cancers11111727.
8
TAM Receptor Pathways at the Crossroads of Neuroinflammation and Neurodegeneration.TAM 受体途径在神经炎症和神经变性的十字路口。
Dis Markers. 2019 Sep 15;2019:2387614. doi: 10.1155/2019/2387614. eCollection 2019.
9
Gas6/TAM System: A Key Modulator of the Interplay between Inflammation and Fibrosis.Gas6/TAM 系统:炎症与纤维化相互作用的关键调节因子。
Int J Mol Sci. 2019 Oct 12;20(20):5070. doi: 10.3390/ijms20205070.
10
Gas6/TAM Signaling Components as Novel Biomarkers of Liver Fibrosis.Gas6/TAM 信号转导组件作为肝纤维化的新型生物标志物。
Dis Markers. 2019 Sep 8;2019:2304931. doi: 10.1155/2019/2304931. eCollection 2019.